Spinal cord injury (SCI) triggers chronic intraspinal inflammation consisting of activated resident and infiltrating immune cells (especially microglia/macrophages). The environmental factors contributing to this protracted inflammation are not well understood; however, myelin lipid debris is a hallmark of SCI. Myelin is also a potent macrophage stimulus and target of complement‐mediated clearance and inflammation. The downstream effects of these neuroimmune interactions have the potential to contribute to ongoing pathology or facilitate repair. This depends in large part on whether myelin drives pathological or reparative macrophage activation states, commonly referred to as M1 (proinflammatory) or M2 (alternatively) macrophages, respectively. Here we review the processes by which myelin debris may be cleared through macrophage surface receptors and the complement system, how this differentially influences macrophage and microglial activation states, and how the cellular functions of these myelin macrophages and complement proteins contribute to chronic inflammation and secondary injury after SCI.
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This work is supported by NIH NINDS R01 NS091582 and the Spinal Cord and Brain Injury Research Center at the University of Kentucky.
Kopper, Timothy J. and Gensel, John C., "Myelin as an Inflammatory Mediator: Myelin Interactions with Complement, Macrophages, and Microglia in Spinal Cord Injury" (2018). Spinal Cord and Brain Injury Research Center Faculty Publications. 31.